Category: 8. Health

Groundbreaking research by the University of Sydney has identified a new brain protein involved in the development of Parkinson’s disease and a way to modify it, paving the way for future treatments for the disease.

With the aim of finding new treatments to slow or stop its progression, the research team has spent more than a decade studying the biological mechanisms underpinning the condition—which is the second most common neurological condition after dementia.

In 2017, they identified for the first time the presence of an abnormal form of a protein—called SOD1—in the brains of patients diagnosed with Parkinson’s disease.

Normally, the SOD1 protein provides protective benefits to the brain, but in Parkinson’s patients it becomes faulty, causing the protein to clump and damage brain cells.

The newest study by the same team, led by Professor Kay Double from the Brain and Mind Centre, was just published in Acta Neuropathologica Communications. It found that targeting the faulty SOD1 protein with a drug treatment using copper improved the motor function in mice.

“We hoped that by treating this malfunctioning protein, we might be able to improve the Parkinson-like symptoms in the mice we were treating – but even we were astonished by the success of the intervention,” said Professor Double in a media release.

“All the mice we treated saw a dramatic improvement in their motor skills, which is a really promising sign that it could be effective in treating people who have Parkinson disease too.

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The study involved two groups of mice with Parkinson-like symptoms. One group was treated with a special copper supplement for three months, while the other received a placebo.

Throughout the study (which was partly funded by the Michael J. Fox Foundation), the mice receiving only the placebo saw a decline in their motor symptoms. The mice receiving the special copper supplement, however, did not develop movement problems.

“The results were beyond our expectations,” said Prof. Double. “They suggest, once further studies are carried out, this treatment approach could slow the progression of Parkinson’s disease in humans.”

At present there is no known cure and only limited treatments for Parkinson’s disease, which is a degenerative disorder in which dopamine-producing cells in the brain die, leading to a range of symptoms including tremors, muscle stiffness, slow movement and impaired balance.

But researchers hope understanding the causes of the disease will lead to improved treatments.

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“As our understanding of Parkinson’s disease grows, we are finding that there are many factors contributing to its development and progression in humans – and faulty forms of the SOD1 protein is likely one of them.

“Just as researchers found with HIV, Parkinson’s disease is a complex condition that likely requires multiple interventions. A single treatment may have a small effect when used alone but, when combined with other interventions, contributes to a significant overall improvement in health.”

The researchers’ next step is to identify the best approach to targeting the faulty SOD1 protein in a clinical trial, which could be the start of a new therapy to slow the development of Parkinson’s disease.

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Pre-hospital blood transfusion has become standard practice in the management of major trauma in the UK, with all 21 UK air ambulance services now carrying blood products. While extensive research has focused on what blood components to give, there remains a notable gap in evidence regarding how transfusion should be administered, particularly with respect to physiological targets like blood pressure and heart rate. Current transfusion strategies are informed by guidelines such as the European and NICE UK guidelines and through courses such as Advanced Trauma Life Support and the European Trauma Courses. These strategies broadly suggest transfusion triggers and targets based on blood pressure and clinical judgement. Current guidelines are based on studies mostly involving fluid—not blood—resuscitation, and acknowledge that existing evidence is limited. Evidence regarding the haemodynamic response to pre-hospital blood transfusion remains sparse. Importantly, there is no strong evidence confirming a linear relationship between transfusion and vital sign improvement, with most existing research on blood product transfusion focusing on ratios and types of product transfused rather than real-time physiological responses to transfusion. Given the complexity and lack of heterogeneity amongst trauma patients clinical decision-making for transfusion is complicated. There are a number of other factors that may cause or contribute to hypotension in trauma in the absence of blood loss; these include Vaso-active head injuries, inflammatory responses and cardiac and endothelial dysfunction. Additional factors such as age, comorbidities, medications, injury mechanism, and frailty influence haemodynamic responses to both trauma and transfusion. In conclusion, while pre-hospital blood transfusion is a critical intervention, understanding its immediate physiological effect on the complex trauma patient remains limited. Future research should explore the haemodynamic response from trauma patients during the immediate transfusion period, reviewing triggers for transfusion and haemodynamic transfusion targets, to ascertain whether there is a linear, predictable physiological response to transfusion resuscitation in the pre-hospital setting.

Mouth and tongue lesions are often one of the first symptoms of human immunodeficiency virus (HIV). HIV weakens your immune system, which can leave you susceptible to sores and infections.

If left untreated, oral health issues can cause pain and other health complications.

Aphthous ulcers are small, yellow or gray sores with a red border. They usually appear on the tongue, cheeks, or inside the lips. Mouth ulcers can make talking and eating painful, especially if they’re located under the tongue.

Mouth ulcers are often a symptom of a weak immune system and stress. An estimated 50% of people with HIV experience mouth and tongue ulcers because of their weakened immune systems. Dry mouth caused by HIV and HIV medications can also increase your risk of mouth sores.

Sores will eventually heal on their own. Mild ulcers can be treated with over-the-counter (OTC) numbing creams that help relieve pain and promote healing. More severe sores are treated with prescription corticosteroid mouthwashes or pills.

Oral thrush is a type of yeast infection that causes patches of creamy white or yellow bumps that coat the tongue. These patches can be painless, or they may burn and bleed. Oral thrush can also affect the tonsils, throat, cheeks, gums, and roof of the mouth. 

Oral thrush is the most common mouth infection that affects people living with HIV. It’s normal for yeast (a type of fungus) to live in your mouth. However, if you have a weakened immune system due to HIV, it’s easier for this fungus to grow too much, leading to infection. Because saliva in the mouth has antibodies to fight infections, HIV-related dry mouth also increases your risk of oral thrush.

Prescription antifungal lozenges, pills, or mouthwashes can treat oral thrush. However, oral thrush often returns if your immune system is too weak.

Oral hairy leukoplakia (OHL) causes white, hair-like patches on the sides of the tongue. It can also appear on the insides of the cheeks and lower lip. These patches can be painless or cause mild pain. In more severe cases, you may lose your sense of taste and experience hot and cold sensitivity.

People with Epstein-Barr virus (EBV)—a common herpes virus—can develop oral hairy leukoplakia. EBV typically infects people with extremely weak immune systems, especially those with HIV. EBV infections are also more common in people with untreated HIV.

Oral hairy leukoplakia patches often go away randomly, but there is no cure for the underlying Epstein-Barr virus. Treatment for OHL may include prescription anti-retroviral medications to help reduce patches and lower EBV in your body. Topical solutions, like podophyllin resin and retinoids, can also be applied to the tongue to remove patches. 

Herpes simplex virus type 1 (HSV-1) can cause swollen, painful sores and blisters on the tongue. Blisters are also common on the lips and the roof of the mouth. Herpes blisters start as small clusters of white or yellow fluid-filled bumps that eventually burst into one larger red sore. 

Oral herpes affects nearly 20% of people with HIV. Living with a weak immune system increases your risk of having more oral herpes outbreaks, which can also spread more easily.

Herpes sores are very contagious and can spread from kissing or sharing utensils. There is no cure for oral herpes, but prescription antivirals can help reduce healing time and future outbreaks.

Oral warts look like small, hard, skin-colored bumps or flat, white growths that resemble cauliflower. These painless warts often appear on the tongue, lips, and inside of the mouth. On the tongue, warts usually look gray or white and grow on the sides of the tongue or the lingual frenulum (the fold underneath your tongue).

Oral warts are caused by different strains of the human papillomavirus (HPV). People with HIV are more likely to get HPV infections and oral warts because of their weakened immune system.

People who are aging with HIV or are doing highly active antiretroviral therapy (HAART) are also at an increased risk of oral warts. Oral warts can be removed surgically or frozen off with cryosurgery. However, warts can come back. 

Oral melanin hyperpigmentation looks like flat, brown patches on the tongue, lips, gums, cheeks, or roof of the mouth. This discoloration is caused by increased melanin (skin pigment) in the mouth.

If you have HIV, the antiretroviral therapy (ART) medication Retrovir (zidovudine), also known as AZT, can cause oral hyperpigmentation as a side effect. HIV-related oral hyperpigmentation doesn’t usually cause problems or require treatment. However, if you’re worried about the appearance of hyperpigmentation, talk with your healthcare provider. You may be able to switch to a different ART medication.

Maintaining good oral hygiene can help prevent HIV tongue and mouth conditions. Some dentist-approved tips include:

• Keep your mouth clean: Brush your teeth for two minutes and floss twice daily to remove food, plaque, and harmful bacteria in your mouth. 
• Visit your dentist regularly: See your dentist at least every six months for cleanings. If you don’t have a dentist, ask your healthcare provider or clinic for a referral. 
• Take your HIV medication: It’s important to take antiretroviral therapy medications as directed and on schedule to reduce HIV in your body and help your immune system recover.
• Avoid dry mouth triggers: Limit things that can lead to dry mouth, like smoking tobacco, drinking alcohol, and eating salty foods.
• Stay hydrated: Drink water often, use a humidifier at bedtime, and consider using toothpaste or mouthwash designed to help dry mouth.

If you have HIV, it’s important to see your provider if you experience any changes in your mouth or tongue. Mouth sores, dry mouth, and oral infections are often indicators that HIV is progressing and the immune system is becoming weaker. Some HIV medications can also make dry mouth worse, so your provider may recommend a different treatment.

If left untreated, oral health complications make you more susceptible to bacterial infections and septicemia (blood poisoning), which can be fatal with a weakened immune system. HIV-related tongue ulcers and dry mouth can cause pain that makes it hard to talk, chew, and swallow. Tongue lesions can also wear down taste buds and cause loss of taste.

Other warning signs of HIV progression that warrant a medical visit include:

• Fatigue
• Fever
• Chills
• Sore throat
• Mouth ulcers
• Rash
• Muscle aches
• Swollen lymph nodes
• Night sweats

The HIV Services Locator is a helpful tool to find qualified healthcare providers in your area.

People with HIV are more likely to have ulcers, oral thrush, dark spots, herpes, and warts that affect the tongue and mouth. Because HIV weakens your immune system and can cause dry mouth, oral health conditions are common.

Practicing good oral hygiene, taking your HIV medications, and visiting your dentist regularly are essential to help prevent complications. 

A new study published in PLOS Pathogens reveals how monkeypox virus (MPXV) and its relatives outsmart the body’s early immune defenses. Infectious disease researchers from Wuhan University and the Wuhan Institute of Virology have discovered that a viral protein called OPG147 plays a key role in helping the virus hide from immune detection during the critical first hours of infection.

OPG147 is part of the machinery that allows poxviruses to enter cells, but this study shows it has a second job: disarming the host’s immune alarm system. The research sheds new light on how MPXV and related poxviruses—including vaccinia virus (VACV), used in smallpox vaccines—avoid triggering a strong antiviral response. These findings could help scientists develop better treatments and safer, more effective vaccines.

The disease caused by monkeypox virus is now officially called mpox, following a 2022 renaming by the World Health Organization to reduce stigma and improve public communication. While mpox refers to the illness, monkeypox virus (MPXV) remains the accepted scientific name for the virus itself.

What Is the MITA/STING Pathway—and Why Does It Matter?

Our bodies rely on innate immunity to recognize infections before symptoms even begin. One of the key systems in this early defense is the MITA/STING pathway. When a virus infects a cell and releases its DNA, a sensor called cGAS detects the foreign material and produces a molecule that activates MITA (also called STING, for STimulator of INterferon Genes). This sets off a chain reaction that results in the production of interferons and other antiviral proteins that help control the infection.

In short: MITA/STING is the body’s built-in alarm system for DNA viruses. Without it, the immune system may not respond quickly enough to stop the virus from spreading.

How the Virus Silences the Alarm

The study shows that OPG147 from monkeypox virus—and similar proteins in other poxviruses—can directly interfere with MITA/STING. OPG147 doesn’t block the initial detection of the virus. Instead, it quietly sabotages the steps needed for MITA/STING to activate a full immune response:

• OPG147 blocks a chemical process called ISGylation that helps MITA become fully active.
• It prevents MITA from forming the structures it needs to send out immune signals.
• It traps MITA inside the cell’s endoplasmic reticulum, stopping it from moving to the places where it would normally raise the alarm.

By interfering with these processes, OPG147 allows the virus to establish infection without alerting the immune system right away.

A Weak Spot in the Virus’s Armor

To test how important OPG147 is for the virus, researchers created a mutated version of vaccinia virus where OPG147 could no longer interact with MITA. They found that this altered virus:

• Triggered stronger immune responses in human cells and in mice.
• Produced lower levels of virus in the body.
• Caused milder disease and less tissue damage.
• Did not lose its ability to replicate, meaning the mutation specifically weakens the virus’s ability to evade immunity—not its basic life cycle.

These results show that OPG147 is a key virulence factor—critical for helping the virus cause disease.

Why This Matters for Public Health and National Security

Although mpox is no longer a rare disease, it continues to pose a public health and global security challenge, especially for immunocompromised individuals and in regions with limited access to vaccines and treatments. In addition, orthopoxviruses remain a concern for potential biosecurity threats.

This research identifies OPG147 as a potential weak point that could be targeted by new antiviral drugs or used to develop safer, more effective vaccines. For public health agencies and global health security planners, this study provides valuable insights into how poxviruses evade immune detection—a crucial piece of knowledge for surveillance, outbreak response, and vaccine development.

A New Direction for Vaccine and Antiviral Strategies

What makes OPG147 especially interesting is that it works differently from other known poxvirus immune blockers. While some viral proteins destroy the molecules that signal an immune response, OPG147 directly jams the signaling machinery, making it harder for the immune system to detect the infection in time.

This strategy shows just how sophisticated viruses can be in evading immune defenses—and it suggests that combining treatments that target multiple viral evasion proteins may offer stronger protection.

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Zhou X, Liu Z, Shi W, et al. The conserved poxvirus membrane entry-fusion apparatus component OPG147 targets MITA/STING for immune evasion. PLOS Pathogens. June 11, 2025.

In a recent analysis led by Ryan Hankins, MD, urologist at MedStar Georgetown University Hospital in Washington, DC, researchers explored a compelling new angle on the use of rectal spacers during prostate cancer radiotherapy. While rectal spacers have long been used to reduce rectal toxicity from radiation therapy, emerging evidence suggests their benefits may extend further, including a potential impact on erectile dysfunction (ED) outcomes.

“We use rectal spacers to help prevent [adverse events] from radiation therapy for prostate cancer. The spacers [were] developed to help with rectal toxicity, primarily to prevent rectal toxicity from radiation therapy. We are seeing now that there may be other benefits,” Hankins explains in an interview with Targeted Oncology^TM.

The study utilized a massive dataset drawn from Medicare and included 247,250 patients with prostate cancer who received radiation therapy between 2015 to 2022. Rather than focusing on individual patient-level data, the team opted for a county-level approach to maximize the reach and scale of the study.

“These are large data sets that are readily available, so this is based on diagnoses that are reported, or really government-reported diagnosis codes, and so we can dive into large data sets to see if we can find associations with improvement in these [adverse events],” he shares.

The analysis revealed a notable association: counties with higher utilization of rectal spacers during prostate cancer radiotherapy showed lower rates of ED diagnoses. While the data is observational and further research is needed to confirm causality, the findings point toward a potentially broader protective role for rectal spacers.

REFERENCE:

Hankins RA, Sato R, Mehta P, Bhattacharyya S, Ezekwekwu E, Collins S. Real-world U.S. county-level analysis of erectile dysfunction diagnosis following radiation therapy for localized prostate cancer: The impact of rectal spacer utilization. J Urol. 2025;213(5S):e1327. doi:10.1097/01.JU.0001110184.48142.9e.03

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A breakthrough at the Massachusetts Institute of Technology (MIT) could soon make sophisticated medical diagnostics as cheap and accessible as a blood glucose test. A research team has developed a 50-cent electrochemical sensor that can detect specific disease genes, and crucially, can be stored for up to two months at room temperature.

The technology uses a DNA-coated electrode and leverages a CRISPR-based enzyme, Cas12. When the sensor encounters a target gene from a virus or cancer cell, the enzyme activates and begins to shred the DNA on the electrode. This action creates a distinct electrical signal, confirming a positive result. While promising, a key challenge has been the fragility of the DNA coating, which previously limited the sensors’ shelf-life to only a few days.

The MIT team, led by Professor Ariel Furst, solved this by applying a simple, inexpensive coating of polyvinyl alcohol (PVA), a common polymer. The PVA acts like a protective tarp, stabilizing the delicate DNA and allowing the sensors to be stored and shipped without refrigeration. After two months in storage at temperatures up to 150 °F (65.56 °C), the team confirmed the sensors could still accurately detect a gene associated with prostate cancer.

Our focus is on diagnostics that many people have limited access to, and our goal is to create a point-of-use sensor. People wouldn’t even need to be in a clinic to use it. You could do it at home. — Professor Ariel Furst.

The versatility of the platform means it can be adapted to test for a wide range of infectious diseases, such as HIV and HPV, and various cancers using samples like urine or saliva. A group from Furst’s lab is now launching a startup through MIT’s delta v accelerator to begin testing the durable sensors with patient samples in real-world environments.

Did you know? H. pylori, a bacterium that has infected more than 50% of the global population, is the leading cause of stomach cancer. It is even classified as a Group 1 carcinogen. The good news is H. pylori infection is treatable — and early diagnosis can significantly lower the risk of cancer. NewPos Self-test Kit (curr. $19.99 on Amazon) can help you do just that.

I have always been fascinated by technology and digital devices my entire life and even got addicted to it. I have always marveled at the intricacy of even the simplest digital devices and systems around us. I have been writing and publishing articles online for about 6 years now, just about a year ago, I found myself lost in the marvel of smartphones and laptops we have in our hands every day. I developed a passion for learning about new devices and technologies that come with them and at some point, I asked myself, “Why not get into writing tech articles?” It is useless to say I followed up the idea — it is evident. I am an open-minded individual who derives an infinite amount of joy from researching and discovering new information, I believe there is so much to learn and such a short life to live, so I put my time to good use — learning new things. I am a ‘bookworm’ of the internet and digital devices. When I am not writing, you will find me on my devices still, I do explore and admire the beauty of nature and creatures. I am a fast learner and quickly adapt to changes, always looking forward to new adventures.

According to McGill University, TissueTinker is using 3D bioprinting to revolutionize cancer drug testing by replacing outdated methods like animal trials and 2D cell cultures. Traditional models fail to mimic the complexity of human tumours, contributing to a staggering failure rate—over 90%—for cancer drugs that pass preclinical tests but flop in human trials.

TissueTinker, a recent McGill Innovation Fund (MIF) awardee, tackles this problem head-on. The startup creates miniaturized tumour models using 3D printing technology—specifically, bioink—to replicate both healthy and diseased human tissue side by side. These printed tumours are as small as 300 microns, the “sweet spot size,” according to co-founder Benjamin Ringler. “It’s large enough that it’s still valuable for testing purposes, but small enough to minimize resources.”

More than just small, these tumours are smart. Researchers can customize them to simulate specific tumour environments, gaining targeted insights into cancer behavior. “The ability to customize the tumour really allows researchers to gain deep, targeted insights into how cancer behaves at a micro level,” Ringler explained. This adaptability improves the predictive power of early-stage testing, reducing wasted investment in drugs that would otherwise fail in clinical trials.

“Because the testing environment more readily simulates the human body, researchers can better assess and understand whether or not their drug works before reaching clinical trial stages,” Ringler added. With development costs topping $1–2 billion per drug, this level of precision is not just a scientific advancement—it’s a financial necessity.

TissueTinker is scaling its technology, backed by the McGill Innovation Fund. “The MIF has provided tailored support, offering specific advice and helping us think critically about not just our next step, but our many steps down the road,” said Ringler. Alongside co-founders Madison Santos and Isabelle Dummer—experts in biomedical engineering and cell therapy—the team plans to expand their tumour model library and eventually license the platform.

“We’re not just solving a problem; we’re rethinking the way we approach cancer drug development,” said Ringler.